LIVER - NON HEPATITIS & Cannabis studies completed

Overview

Like any other medicinal plant,
cannabis has intrinsic properties that allow it to produce both
beneficial effects and undesired side effects.

Some
of these side effects are cognitive, such as the impairment of the
short-term memory or the potential to trigger psychotic episodes in
susceptible individuals. (Sensi Seeds published an interesting article
on Cannabis and Episodic Memory. To read it click here, ed)

The
negative physical side effects of cannabis include an increase in
oxygen consumption by the heart tissues and, as we shall see in this
article, the capacity to accelerate the progression of fibrosis in individuals suffering chronic Hepatitis C, if cannabis is consumed regularly and not just on a sporadic basis.

In cirrhotic
human livers, there is a higher number of CB1 Cannabinoid receptors,
which indicates that the Endocannabinoid system is involved in the
physiopathology of this clinical picture. (You can read more about the
Cannabinoid Science and the Endocannabinoid System here, ed)

BACKGROUND/AIMS: The endocannabinoid system in mice plays a role in models of human cirrhosis and hepatic encephalopathy (HE), induced by a hepatotoxin. We report now the therapeutic effects of cannabidiol (CBD), a non-psychoactive constituent of Cannabis sativa, on HE caused by bile duct ligation (BDL), a model of chronic liver disease.

METHODS: CBD (5mg/kg; i.p.) was administered over 4weeks to mice that had undergone BDL. RESULTS: Cognitive function in the eight arm maze and the T-maze tests, as well as locomotor function in the open field test were impaired by the ligation and were improved by CBD. BDL raised hippocampal expression of the TNF-alpha-receptor 1 gene, which was reduced by CBD. However, BDL reduced expression of the brain-derived neurotrophic factor (BDNF) gene, which was increased by CBD. The effects of CBD on cognition, locomotion and on TNF-alpha receptor 1 expression were blocked by ZM241385, an A(2)A adenosine receptor antagonist. BDL lowers the expression of this receptor.

CONCLUSIONS: The effects of BDL apparently result in part from down-regulation of A(2)A adenosine receptor. CBD reverses these effects through activation of this receptor, leading to compensation of the ligation effect.

In addition, the results showed that eCBD increased the reduced glutathione (GSH) content in the liver leading to a restoration of the defence mechanism and significantly decreased the liver lipid peroxidation suggesting that eCBD provides protection against oxidative damage in STZ-induced diabetes that also strongly contributes to the development of neuropathy.

Finally, the nerve growth factor content in the sciatic nerve of diabetic rats was restored to normal following the repeated treatment with eCBD, suggesting that the extract was able to prevent the nerve damage caused by the reduced support of this neurotrophin.

These findings highlighted the beneficial effects of cannabis extract treatment in attenuating diabetic neuropathic pain, possibly through a strong antioxidant activity and a specific action upon nerve growth factor.